SSRIs Are Drugs, Too

Antidepressant treatment should be judged by durable improvement in the patient’s life, including function, independence, emotional responsiveness, sexual health, and the ability to leave treatment when appropriate. This Perspective reviews evidence for acute SSRI benefit, maintenance effects, withdrawal, persistent adverse outcomes, and the limits of short-duration trials relative to years of prescribing. It advances a falsifiable Dynamic-Reserve hypothesis: in a susceptible subgroup, depressive and multisystem symptoms arise from constrained thiamine-dependent cerebral capacity; an SSRI may restore selected functions without correcting that constraint and may accelerate decline in effective metabolic reserve during sustained exposure. The model predicts early clustering of insomnia, anxiety, irritability, and tremor; additional autonomic, peripheral, or ocular signs in selected patients; treatment-related divergence between symptom scores and whole-person recovery; and increased difficulty discontinuing medication when Borrowed Function and physiological adaptation coexist. An operational definition of addiction based on loss of practical exit control is proposed. Experimental thiamine-transporter interactions and mitochondrial findings provide partial biological rationale but do not demonstrate the proposed patient-level causal chain. The manuscript distinguishes the broad reserve hypothesis from a thiamine-specific mechanism and specifies observations capable of falsifying both.